Many aspects of the physiological stress related to the exposure to the hyperbaric environment have been studied, but no research has been made to evaluate the impacts of scuba diving on heart rate variability (HRV). We investigated the effects of a simulated dive to 557 KPa (45 meters of salt water) for a 30-minute bottom time on the frequency and time domains estimators of HRV. Electrocardiogram records were obtained with superficial electrodes for 30 minutes before the simulated dive and, subsequently, for one hour after the dive. Each of these time-series was then subdivided into non-overlapping windows of 256 consecutive R-R in- tervals. A control group was submitted to the same proto- col, breathing the same gases used in the simulated dive, while not being exposed to the hyperbaric environment. In the control group we observed a significant increase in SDNN (the square root of the variance of the R–R intervals), RMSSD (the square root of the mean squared differences of successive R-R intervals), and in two bands (high and low) of the power spectrum of frequencies. The subjects in the simulated dive presented only an increase in the low frequency estimator without any further relevant changes in other estimators of HRV. This study suggests that the low frequency increase without concomitant high frequency increase might be an indicator of the physiological stress caused by decom- pression and that such a dissimilarity in responses might be correlated to the dive-related impairment of the endothelial function.

Histidine-containing dipeptides (HCDs) are abundantly expressed in striated muscles. Although important properties have been ascribed to HCDs, including H + buffering, regulation of Ca 2+ transients and protection against oxidative stress, it remains unknown whether they play relevant functions in vivo . To investigate the in vivo roles of HCDs, we developed the first carnosine synthase knockout (CARNS1 −/− ) rat strain to investigate the impact of an absence of HCDs on skeletal and cardiac muscle function. Male wild-type (WT) and knockout rats (4 months-old) were used. Skeletal muscle function was assessed by an exercise tolerance test, contractile function in situ and muscle buffering capacity in vitro . Cardiac function was assessed in vivo by echocardiography and cardiac electrical activity by electrocardiography. Cardiomyocyte contractile function was assessed in isolated cardiomyocytes by measuring sarcomere contractility, along with the determination of Ca 2+ transient. Markers of oxidative stress, mitochondrial function and expression of proteins were also evaluated in cardiac muscle. Animals were supplemented with carnosine (1.8% in drinking water for 12 weeks) in an attempt to rescue tissue HCDs levels and function. CARNS1 −/− resulted in the complete absence of carnosine and anserine, but it did not affect exercise capacity, skeletal muscle force production, fatigability or buffering capacity in vitro , indicating that these are not essential for pH regulation and function in skeletal muscle. In cardiac muscle, however, CARNS1 −/− resulted in a significant impairment of contractile function, which was confirmed both in vivo and ex vivo in isolated sarcomeres. Impaired systolic and diastolic dysfunction were accompanied by reduced intracellular Ca 2+ peaks and slowed Ca 2+ removal, but not by increased markers of oxidative stress or impaired mitochondrial respiration. No relevant increases in muscle carnosine content were observed after carnosine supplementation. Results show that a primary function of HCDs in cardiac muscle is the regulation of Ca 2+ handling and excitation-contraction coupling.

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